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Cardiovascular and Pulmonary > Acid-Base regulation II > Flashcards

Acid-Base regulation II Flashcards

1
Q

The effectiveness of respiratory compensation for metabolic acidosis is limited to several days at best. This is because lowering PCO2 has what effects?

A

Increases pH, reduces renal HCO3- reabsorption (which then lowers plasma HCO3-)

Net effect is as if no compensation has occurred at all

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2
Q

Predicted respiratory compensation for metabolic acidosis is a

A

1.5 mmHg drop in PCO2 per 1 meq/L decrease in HCO3-

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3
Q

Useful to determine whether or not appropriate respiratory compensation to metabolic acidosis has occurred versus the presence of a second (respiratory) based acid-base disorder

A

Winter’s Formula

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4
Q

Using Winter’s formula, if the calculated and measured PCO2 values are equal than we know that

A

Appropriate compensation is occuring

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5
Q

Using Winter’s formula, if the measured PCO2 is greater than the calculated PCO2, than we know there is either

A

Respiratory acidosis too or no compensation

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6
Q

Is a PCO2 of 40 mmHg in the presence of a metabolic acidosis normal?

A

NO

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7
Q

With a chronic metabolic acidosis, any PCO2 value significantly above what Winter’s predicts would indicate a

A

Co-existing respiratory acidosis

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8
Q

With a chronic metabolic acidosis, a measured PCO2 less than calculate by Winter’s formula reveals the presence of co-existing

A

Respiratory alkalosis

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9
Q

A normal pH with abnormal ABGs should immediately raise suspicion of a

A

Mixed acid-base disorder

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10
Q

The final compensatory mechanism for metabolic acidosis is via the

A

Renal acidification of urine

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11
Q

Assuming the kidneys are functioning normally, this process can begin within about 24 hours and is maximal at approximately

A

5-6 days

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12
Q

Renal compensation for metabolic acidosis predominantly involves enhanced elimination of

A

NH4+ (as NH4Cl)

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13
Q

As an example of the effectiveness of the kidneys in handling an increased acid load, a reduction of plasma HCO3- by only 4-5 meq/L can result in a

A

4-fold increase in NH4+ excretion over several days

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14
Q

Determined by calculating the difference between the predominant plasma cation (Na+) and the sum of the most abundant plasma anions (HCO3- and Cl-)

A

Anion gap (AG)

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15
Q

The normal range for AG is

A

7-16 meq/L

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16
Q

The AG is simply the difference between

A

Unmeasured cations - unmeasured anions

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17
Q

Accounts for the majority of unmeasured anions

A

Negative charges within proteins

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18
Q

Therefor, an increased gao can result from a fall in unmeasured cations, or (most often) an increase in

A

Unmeasured anions

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19
Q

An important unmeasured anion to note is

A

Albumin

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20
Q

In the case of hemoconcentration, where the concentration of albumin is increased, the anion gap would be

A

Elevated

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21
Q

In the event of hypoalbuminemia, for every 1g/dL drop in plasma albumin, AG should be adjusted downward by

A

2.5 meq/L

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22
Q

The accumulation of certain anions can occur during various types of

A

Metabolic acidoses

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23
Q

Elevated AG ALWAYS strongly suggests the presence of

A

Metabolic acidosis

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24
Q

Duringmetabolic acidosis, and in the absence of unmeasured anions, lost HCO3- is replaced in order to maintain electroneutrality. What replaces it?

A

Cl-

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25
Q

This normal anion gap metabolic acidosis is often referred to as

A

Hyperchloremic metabolic acidosis

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26
Q

Common with normal AG metabolic acidosis

A

Hyperchloremia

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27
Q

HCl + NaHCO3 → NaCl + H2CO3 → CO2 + H2O

In this example, what is the result of loss of NaHCO3 due to a GI pathology?

A

Metabolic acidosis from increase in HCL due to loss of NaHCO3-

HCl is buffered by remaining HCO3- which results in increased Cl-

Results is hyperchloremia with normal AG

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28
Q

However, if H+ were to combine with an unmeasured anion, than what would happen?

A

AG would be elevated

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29
Q

With this in mind, it is not unusual for plasma chloride to be lowered with an

A

AG metabolic acidosis

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30
Q

It is important to note that increased AG is not exclusive to metabolic acidosis and can occur during

A

Metabolic alkalosis

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31
Q

The main factors contributing to this are

A
  1. ) ECV depletion (contraction alkalosis) causing increased plasma [albumin]
  2. ) Increase lactate production
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32
Q

Can occur in compensation for alkalemia

A

Increased lactate production

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33
Q

Lactic acid, ketoacids, salicylic acid, oxalic acid, glycolic acid, and formic acid each carry negative charges, and will each induce an abnormal rise in

A

AG (causing metabolic acidosis)

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34
Q

ANother way to show the relationships between anionic acid accumulation and HCO3- loss

A

delta-delta difference

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35
Q

By convention, we set basal HCO3- to

A

24

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36
Q

By convention, we set the normal AG to be

A

12

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37
Q

What is the delta-delta difference?

A

dd = Measured AG + measured [HCO3-] - 36

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38
Q

If dAG - dHCO3- = 0 than there is a single acid-base disorder which is

A

Metabolic acidosis

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39
Q

If there is a 1:1 correlation between dAG and dHCO3-, i.e. dAG - dHCO3- = 0 +/- 5 than we have

A

Ketoacidosis

40
Q

We have to calculate the dd difference in a different manner for

-due to the way lactate is cleared by the kidneys

A

Lactic acidosis

41
Q

When we calculate dd diference during lactic acidosis, we know there is a SINGLE metabolic acid-base disorder if the value falls within

A

0 +/- 5

42
Q

With the aforementioned in mind, dd values less than -5 warrant investigation for the presence of a

A

Mixed AG metabolic acidosis w/ non-AG metabolic acidosis

43
Q

If dd is greater than 5, than we likely have a mixed

A

Metabolic acidosis with metabolic alkalosis

44
Q

A mixed metabolic acidosis and metabolic alkalosis can occur during severe diabetic ketoacidosis where marked elevated ketones induce

A

Vomiting

45
Q

Derived from pyruvic acid mostly from the processes of glycolysis or the deamination of alanine

A

Lactic acid (lactate + H+)

46
Q

Lactic acid is buffered by HCO3- to yield lactate, which is subsequently metabolized into

A

Pyruvate

47
Q

Pyruvate can then be further metabolized into

A

CO2 + H2O or glucose

48
Q

Either metabolic pathway results in the generation of new

A

HCO3-

49
Q

The catalysis of lactate requires its entry into the mitochondria and oxidative metabolism, processes which each require sufficient

A

O2

50
Q

Thus, if O2 delivery is blocked, we can see the accumulation of

A

Lactic acid

51
Q

Common causes are poor tissue perfusion leading to impaired oxidation and ischemia, such as what
results from cardiac arrest, shock, severe exercise, alcoholism, and many other pathologies

A

O2 delivery blockages that results in lactic acid buildup

52
Q

During starvation, or perceived starvation, increased lipolysis results in an overabundance of

A

Free fatty acids delivered to the liver

53
Q

Results in elevated serum glucagon and low serum insulin

A

Starvation

54
Q

Caused by a lack of insulin or insulin resistance

A

Perceived starvation

55
Q

In the face of this barrage, hepatic function resets leading to the preferential metabolism of FFA into

A

Ketoacids (rather than the preferred triglycerdies)

56
Q

Signs of hyperglycemia with ketones in the urine correlate with

A

Diabetic ketoacidosis

57
Q

Is measured as the difference between major urinary cations (Na+ and K+) and the major urinary anion (Cl-)

A

Urine AG

58
Q

How do we calculate urine AG?

A

UAG = UNa + UK - UCl

59
Q

Under normal conditions, urine AG will be at or very close to

A

Zero

60
Q

Urine AG can be useful in discerning the cause of

A

Normal AG metabolic acidosis

61
Q

Not useful with elevated AG acidosis

A

Urine AG

62
Q

The most common cause of normal AG metabolic acidosis (due to GI loss of HCO3-)

A

Diarrhea

63
Q

When pH drops, the kidneys will excrete H+ in the form of

A

NH4+

64
Q

This so-called acidification of urine occurs in the distal portions of the structures known as

  • Where urine is being formed
  • Called distal acidification
A

Nephrons

65
Q

Excreted with H+ in order to maintain electroneutrality

A

Cl-

66
Q

Thus, if the kidneys are doing their job in response to metabolic acidosis, excreted urine will contain a lot of Cl- and this drives

A

Urine AG to negative values

67
Q

A negative AG is usually in the range of

A

-20 to -50 meq/L

68
Q

Acidoses that result from the inability of the kidneys to properly acidify urine

A

Renal Tubule Acidoses (RTA)

69
Q

In an RTA, because H+ is not effectively cleared by the kidneys, the ratio of plasma HCO3-/H+ decreases and pH drops, thus forming a

A

Metabolic acidosis

70
Q

Since these kidneys are sick, they can not excrete the excess H+, which means they will not excrete Cl- either, and this drives

A

Urine AG to positive values

71
Q

An elevation in plasma [HCO3-] due to H+ loss

A

Metabolic alkalosis

72
Q

Caused by diarrhea, antacid therapy, hypovolemia, vomiting, and nasogastric suction

A

Metbolic alkalosis

73
Q

Contraction alkalosis around a set amount of HCO3-

-A concern with diuretic usage

A

Hypovolemia

74
Q

The maintenance of metabolic alkalosis usually involves a defect in renal HCO3- secretion and excretion due to

A

Effective volume depletion and Cl- loss

75
Q

Impeded due to excess HCO3-

A

Cl- resorption from the kidneys

76
Q

The kidneys respond to volume depletion by increasing the reabsorption of

A

Na+

77
Q

This process is mediated by

A

Aldosterone and An-II

78
Q

In the context of volume depletion and metabolic alkalosis, An-II stimulates

A

Aldosterone secretion

79
Q

An-II also acts with the kidneys to stimulate the

A

Proximal Na+/H+ exchanger and the Na+/HCO3- symporter

80
Q

Remember that H+ secretion equates to

A

HCO3- reabsorption by the kidneys

81
Q

Thus with elevated An-II, K+ secretion is upregulated (via aldosterone) and HCO3- reabsorption is

A

Directly enhanced

82
Q

Signs of hypokalemia and hypochloremia often accompany

A

Metabolic alkalosis

83
Q

To be more specific, to compensate for volume depletion, the kidneys attempt to increase the resorption of

A

Na+ and Cl-

84
Q

It is important to understand that this process is coupled. In other words

A

There is a 1:1 ratio between Na+ resorption and Cl- resorption

85
Q

With reduced Cl-, Na+ resorption can only occur at the expense of

A

K+ and H+ secretion

86
Q

H+ secretion equates to increased HCO3- resorption and the alkalosis can be exacerbated by

A

K+ loss

87
Q

In order to compensate for metabolic alkalosis, pH must be lowered , and this is accomplished via

-opposite of what is seen in metabolic acidosis

A

Decreased ventilation

88
Q

In acid-base disturbances, we can see shifts between H+ and the most abundant intracellular cation

A

K+

89
Q

There is a connection between metabolic alkalosis and

A

Hypokalemia

90
Q

At the cellular level, increased extracellular pH (low [H+]) results in?

-The reason hypokalemia is associated with metabolic alkalosis

A

H+ translocating from cells to ECF. This is offset by K+ moving from ECF into cells. Thus ECF [K+] is decreased and we can see hypokalemia

91
Q

How does hypokalemia result in metabolic alkalosis?

A

Low K+ causes K+ to move from cells to ECF. To maintain electroneutrality, H+ then moves from ECF into cells and the result is an increased pH

92
Q

Abnormally increased K+ excretion may induce metabolic alkalosis, and hypokalemia actually promotes

A

Renal H+ secretion

93
Q

The trade-off for H+ secretion is the generation and absorption of

A

HCO3-

94
Q

Volume contraction, diminished glomerular filtration rate, and aldosterone excess often accompany

A

Metabolic alkalosis

95
Q

Renal H+ secretion is stimulated by which three things?

A
  1. ) Aldosterone excess
  2. ) Hypovolemia
  3. ) Hypokalemia
96
Q

How does acidosis result in hyperkalemia?

A

Acidosis impairs renal tubular K+ secretion and K+ excretion is diminished.

Increased extracellular H+ causes H+ to move into cells which results in K+ moving to the ECF to maintain electroneutrality

97
Q

Hyperkalemia and acidosis are often coupled because hyperkalemia suppresses

A

H+ secretion from kidneys

Cardiovascular and Pulmonary (25 decks)

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